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Diabetes Mellitus - Type 2

   

Added on  2019-10-30

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Diabetes Mellitus- Type 2 DIABETES MELLITUS - TYPE 21

Diabetes Mellitus- Type 2 Diabetes Mellitus (DM) - Type 2Despite health-care advancements, Type-2 DM is still one among the cause forpremature-morbidity as well as mortality rates. According to International- Federation ofDiabetes (2014), Diabetes was found to have affected 371 millions (prevalence-rate: 8.3%)worldwide in 2012 with 90% of type-2 DM to 422 millions in 2014(WHO, 2017). Thepercentage was estimated to rise to 552 million populations with a prevalence rate of 9.9% by2030 which is mainly due to the increasing diabetic burden specifically in developing nations(Hill, 2013). In-regard to US, the number of diabetic cases have raised from 23.6 million in 2007to approximately 25.8 million in 2011. The objective of this post is to discuss the etiological withrisk factors, pathophysiology, clinical manifestations, diabetic-complications and diagnostic testsfor Type-2 DM.Though the exact cause is unknown, polygenic-gene mutations of MODY-1, 2 and 3 mayincrease DM risk. The 3 metabolic abnormalities that related with type-2 DM are: 1) insulinresistance- unresponsiveness of bodily tissues to insulin action; 2) decreased ability of pancreasto secrete insulin (fatigue of β-cells) and 3) inappropriate production of glucose by liver. Otherrisk-factors include uncontrolled growth of population, central obesity, advanced age,westernization/urbanization, ethnicity, familial history, unhealthy food intake, sedentary life-style, polycystic-ovarian syndrome and gestational diabetes (Pratley, 2013). Type-2 DM is highly complex as well as progressive disease that is characterized withvaried metabolic abnormalities affecting multiple organ-systems (Fig: 1, Appendix-1). The majordefects that contributes to the type-2 DM development involves decreased secretion of insulin aswell as resistance of body-tissues as adipose-tissues, muscles with liver for insulin. The impairedinsulin secretion occurs because of the gradual reduction of the pancreatic β-cellular function2

Diabetes Mellitus- Type 2 along with decreased β-cellular mass. Only 20% of β-cells were found to function at the time ofdiagnosis (Pratley, 2013). The progression of hyperglycemia may also impair the functioning ofβ-cells and secretion of insulin. Moreover, increased production of liver-glucose (reduced insulinaction) with excess glucagon-production and altered incretin-effect plays a role in DMpathophysiology. The hormones such as GLP-1 (glucagon-like peptide-1) that inhibits β-cellularapoptosis and GIP (glucose dependent insulin-tropic-polypeptide) controls incretin- effect, aprocess in which the secretion of insulin increases in-response to oral glucose than that ofintravenous glucose. The incretin-effect will be altered in type-2 DM patients, specifically due tothe altered effect of GLP-1 with GIP (Pratley, 2013). The classic features of type-2 DM include polyuria and polydipsia that occurs due toosmotic effect of glucose and polyphagia that occurs due to cellular malnourishment. Otherfeatures include increased fatigue because of glucose deprivation, blurred vision, frequentinfections, delayed wound healing, weight loss and acanthosis nigricans (sign indicating insulin-resistance). These features appear gradually and the manifestations may not occur tillcomplication occurs. Varied complications as retinopathy, angiopathy, neuropathy, nephropathyand frequent infections may arise if Type-2 DM is uncontrolled. DM increases risk for cardio-vascular diseases because of diabetic-angiopathy that accounts for 65% of DM-based deaths.Type-2 DM patients are found to have 2-6 times increased risk for stroke and 2-8 times forcardiac-failure (Pratley, 2013). Diabetic-retinopathy is the main cause for blindness in persons aged 20-74 years (IDF,2014, Bourne, 2013). Diabetic-nephropathy that affects 40% of Type-2 DM patients is themainetiology of chronic-renal disease and diabetic-neuropathy that affects 50% of DM adultsincreases the chance of developing foot-ulcers and limb-amputation (Tesfaye, 2012, Singh,3

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